Evidence map›Paper›PMID 27039663›Full record

ArticleBiochimica et biophysica acta2016

AKAP-9 promotes colorectal cancer development by regulating Cdc42 interacting protein 4.

Zhi-Yan Hu, Yan-Ping Liu, Lin-Ying Xie, Xiao-Yan Wang, Fang Yang, Shi-You Chen, Zu-Guo Li

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
4.2field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Zhi-Yan HuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Guangzhou 510515, China.
Yan-Ping LiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Guangzhou 510515, China.
Lin-Ying XieDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Guangzhou 510515, China.
Xiao-Yan WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Guangzhou 510515, China.
Fang YangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Guangzhou 510515, China.
Shi-You ChenDepartment of Physiology & Pharmacology, University of Georgia, Athens, GA, United States. Electronic address: sc229@uga.edu.
Zu-Guo LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China; Guangdong Provincial Key Laboratory of Molecular Tumour Pathology, Guangzhou 510515, China. Electronic address: Lizg@smu.edu.cn.
Key Laboratory of Guangdong Province · CNUniversity of Georgia · US

Funding

Novel mechanism of smooth muscle phenotypic modulation and vascular remodelingR01HL119053 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI CHEN, SHIYOU · 2014 to 2023
$3.8M
Dedicator of Cytokinesis 2 in smooth muscle phenotype modulationR01HL123302 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI CHEN, SHIYOU · 2014 to 2018
$1.8M
Smooth Muscle Differentiation and MaturationR01HL107526 · NHLBI · UNIVERSITY OF GEORGIA · PI CHEN, SHIYOU · 2011 to 2014
$1.5M
NHLBI NIH HHS R01 HL107526NHLBI NIH HHS R01 HL119053NHLBI NIH HHS R01 HL123302
6 · The paper itself

Abstract

Our previous studies have shown that PRKA kinase anchor protein 9 (AKAP-9) is involved in colorectal cancer (CRC) cell proliferation and migration in vitro. However, whether or not AKAP-9 is important for CRC development or metastasis in vivo remains unknown. In the present study, we found that AKAP-9 expression was significantly higher in human colorectal cancer tissues than the paired normal tissues. In fact, AKAP-9 level correlated with the CRC infiltrating depth and metastasis. Moreover, the higher AKAP-9 expression was associated with the lower survival rate in patients. In cultured CRC cells, knockdown of AKAP-9 inhibited cell proliferation, invasion, and migration. AKAP-9 deficiency also attenuated CRC tumor growth and metastasis in vivo. Mechanistically, AKAP-9 interacted with cdc42 interacting protein 4 (CIP4) and regulated its expression. CIP4 levels were interrelated to the AKAP-9 level in CRC cells. Functionally, AKAP-9 was essential for TGF-β1-induced epithelial-mesenchymal transition of CRC cells, and CIP4 played a critical role in mediating the function of AKAP-9. Importantly, CIP4 expression was significantly up-regulated in human CRC tissues. Taken together, our results demonstrated that AKAP-9 facilitates CRC development and metastasis via regulating CIP4-mediated epithelial-mesenchymal transition of CRC cells.

Indexed as

A Kinase Anchor ProteinsAnimalsCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsCytoskeletal ProteinsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMice, Inbred BALB CMice, NudeMicrotubule-Associated ProteinsMiddle AgedMinor Histocompatibility AntigensNeoplasm InvasivenessAKAP9 protein, humanA Kinase Anchor ProteinsCytoskeletal ProteinsMicrotubule-Associated ProteinsMinor Histocompatibility AntigensTRIP10 protein, humanAKAP-9Cdc42 interacting protein 4Colorectal cancerEpithelial-mesenchymal transitionMetastasis

Identifiers

PMID27039663
PMCPMC4846471
OpenAlexW2341649826

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.